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Reoviruses and the host cell

K L Tyler1, P Clarke, R L DeBiasi

  • 1Dept of Neurology, University of Colorado Health Sciences Center, Campus Box B-182, 4200 E, 9th Avenue, Denver, CO 80262, USA. Ken.Tyler@UCHSC.edu

Trends in Microbiology
|February 5, 2002
PubMed

Insights

Reovirus infection disrupts cell cycles and triggers apoptosis by interacting with junctional adhesion molecule (JAM). This interaction activates specific signaling pathways, influencing cell death and immune responses.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Reovirus infection impacts host cell cycle regulation and induces programmed cell death (apoptosis).
  • Specific reovirus strains exhibit varying abilities to cause cell cycle arrest and apoptosis, linked to the viral S1 genome segment.
  • Reovirus-induced apoptosis involves tumor necrosis factor (TNF) superfamily death receptors and caspase activation.

Purpose of the Study:

  • To investigate the role of junctional adhesion molecule (JAM) as a reovirus receptor.
  • To elucidate the mechanisms by which reovirus binding to JAM influences apoptosis and NF-kappaB activation.

Main Methods:

  • Analysis of reovirus-host cell interactions.
  • Mapping of viral genome segments responsible for cell cycle and apoptosis induction.
  • Investigation of mitogen-activated protein kinase (MAPK) and nuclear factor-kappaB (NF-kappaB) signaling pathways.

Main Results:

  • The viral S1 genome segment dictates differences in cell cycle arrest (G1 and G2/M phases) and apoptosis induction among reovirus strains.
  • Reovirus infection activates both death receptor and mitochondrial-associated caspases.
  • Junctional adhesion molecule (JAM) is identified as a novel reovirus receptor, crucial for apoptosis and NF-kappaB activation.

Conclusions:

  • Reovirus binding to JAM is essential for initiating apoptosis and activating NF-kappaB.
  • Further research is needed to fully define the cellular pathways mediating JAM-dependent reovirus effects.

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